It has become clear that a reduction in
sex hormones from middle age onwards, increasing age, and an increase in oxidative stress related to lifestyle-related diseases can also reduce bone material properties in terms of
collagen post-translational modification, crosslink formation. These changes lead to both qualitative and quantitative abnormalities in
collagen, which is the major bone matrix
protein. The intermolecular cross-link formation of
collagen, which regulates bone-material attributes, is a mechanism independent of bone remodeling. In other words, cross-link formation is controlled by the environment surrounding the bone matrix, comprising cellular functions, oxidative stress, and glycation level. Because oxidative stress is also risk factor of
arteriosclerosis and cardiovascular event, there is link between low bone quality and
arteriosclerosis. High levels of
pentosidine in urine or blood, or mild
hyperhomocysteinemia which suggest bone
collagen abnormalities, might be used as
surrogate markers for evaluating bone quality, assessing the risk of
bone fracture. Patients with
osteoporosis can be divided into 3 types on the basis of bone density and with bone quality. We are entering an age in which the treatment of
osteoporosis will be personalized, with drugs administered depending on these types.